General Rheumatology   

Are there specific immunosuppressive agents effective for this manifestation?

SLE, APLS, Sjogrens, and RA can sometimes have associated serum hyperviscosity. Is the standard viscosity test sensitive enough for these conditions a...

Renal perfusion scan shows 14 % perfusion on affected side. 

No history of malignancy. No Raynauds. 

Patient with +ANA 1:2560 for >10 years; rest of serologies are negative. Complements are normal. Negative dsDNA. Antiphospholipid labs are negative...

Patient with long standing history of HLAB27 associated uveitis on adalimumab and new diagnosis of CLL.  

A patient on meloxicam for LBP developed high, persistent fevers and no other symptoms. An IGRA, among many tests, was sent. The IGRA’s mitogen ...

How often does this occur and does this lower your suspicion for a "true" or clinically significant lupus anticoagulant?

The patient has tried conservative measures with compression stockings.

Synovial fluid analysis: cell count >100,000, > 80% neutrophils. Gram stain, cultures (including fungal and mycobacterial), synovial biopsy, and...

Do you generally recommend anti-diarrheals, dietary modifications, or consider this an unacceptable side effect and move to other therapies? 

UpToDate recommends Hydroxychloroquine for all SLE patients, but neutropenia is sometimes ascribed to HCQ rather than the underlying disease. What lev...

Can nodular scleritis be a presenting manifestation of GCA?

What imaging do you use to monitor disease activity? Imaging only shows chronic, fibrotic lesions making it hard to assess disease activity.

What nuances do adult rheumatologists need to understand about pediatric diseases? 

Is there any concern for drug interactions of DMARDs and/or biologics with anti seizure medications?

E.g., a patient with newly diagnosed CIDP who is wheelchair-bound.

Is the diagnosis of Sjogren's mostly clinical in a patient with a consistent history and physical with positive serologies?

Does your choice of DMARD/biologics change due to increased risk of malignancy?

Is there utility when classic inflammatory markers (ESR,CRP) or disease specific markers (C3, C4, dsDNA) do not correlate with patients disease activi...

Thrombocytopenia is moderate (80-100,000 microL). No concomitant cytopenias present.

Would you obtain renal biopsy first or treat with additional immunosuppression for suspected renal involvement related to IgG4?

For example, in patients who are HbSAg negative, anti-HBc positive and HbSAb negative, does vaccination reduce reactivation risk?

Assuming no symptoms of TB, should patients be treated for latent TB prior to starting TNF inhibitors or other immunosuppressive agents?

How should IVIG and either biologic injections or infusions be spaced?

And if so, what is your approach to the diagnosis?

Patient is asymptomatic. Labs showed +P-ANCA 1:160. Negative MPO and PR3.

How do you approach de-escalation or justify therapy maintenance? Do you have tiers of medications that you attempt to de-escalate first? In one parti...

Patient with nephrotic range proteinuria, but there is no evidence of active TMA on renal biopsy.

How do you differentiate symptoms related to centralized pain syndrome from possible cognitive dysfunction?

Are there any instances where you would prefer a biosimilar rather than the reference product? 

Would the etiology of the thrombocytosis play a role in your decision-making?

ANA and ENA negative

Do you wait 12 weeks for confirmation to begin treatment if patient is declining?

Do you just use antibiotic prophylaxis if therapy is started prior to meningococcal vaccination?

Patient has no current evidence of underlying vasculitis or malignancy.

Does your evaluation hinge on nonresolution with warming? How extensive is your workup?

Such as oral methylprednisolone, dexamethasone, prednisolone, etc.

Does treatment with B-cell depletion and/or negative anti-spike antibody status despite COVID mRNA vaccination influence your decision?

Specifically, how do you treat the delayed headache, not the headache that develops during the infusion where pre-hydration and slowing down the rate ...

Would you consider this for patients on B-cell depleting therapies or more broadly for other immunosuppressive agents?

Would you have a different opinion based on whether it is a new therapy or an existing and previously well-tolerated therapy for the patient?

Are there specific features that suggest drug-induced uveitis versus de novo uveitis?

There is some emerging evidence that there is an inflammatory component. 

To my understanding, sm/RNP should also be positive in this situation (and one would assume a positive ANA as well)